Background: Colorectal cancer (CRC) is the third most common cancer worldwide, characterized by a multifactorial etiology including genetics, lifestyle, and environmental factors including microbiota composition. To address the role of microbial modulation in CRC, we used our recently established mouse model (the Winnie-APC) combining inflammation and genetics.
Methods: Gut microbiota profiling was performed on 8-week-old Winnie-APC mice and their littermates by 16S rDNA gene amplicon sequencing. Moreover, to study the impact of dysbiosis induced by the mother's genetics in ACF development, the large intestines of APC mice born from wild type mice were investigated by histological analysis at 8 weeks.
Results: ACF development in 8-week-old Winnie-APC mice was triggered by dysbiosis. Specifically, the onset of ACF in genetically predisposed mice may result from dysbiotic signatures in the gastrointestinal tract of the breeders. Additionally, fecal transplant from Winnie donors to APC hosts leads to an increased rate of ACF development.
Conclusions: The characterization of microbiota profiling supporting CRC development in genetically predisposed mice could help to design therapeutic strategies to prevent dysbiosis. The application of these strategies in mothers during pregnancy and lactation could also reduce the CRC risk in the offspring.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7828790 | PMC |
| http://dx.doi.org/10.3390/cancers13020283 | DOI Listing |
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